Simultaneous Study of Mechanical Stretch-Induced Cell Proliferation and Apoptosis on C2C12 Myoblasts

Abstract

Mechanical stretch may cause myoblasts to either proliferate or undergo apoptosis. Identifying the molecular events that switch the fate of a stretched cell from proliferation to apoptosis is practically important in the field of regenerative medicine. A recent study on vascular smooth muscle cells illustrated that identification of these events may be achieved by addressing the stretch-induced opposite cellular outcomes simultaneously within a single investigation. To define conditions or a model in which both proliferation and apoptosis can be studied at the same time, we exposed in vitro cultured C2C12 myoblasts to a cyclic mechanical stretch regimen of 15% elongation at a stretching frequency of 1 Hz for 0, 2, 4, 6, or 8 h every day, consecutively, for 3 days. Both proliferation and apoptosis were observed. Moreover, as the duration of the stretch was prolonged, cell proliferation increased until it peaked at the optimal stretching duration. Afterwards, apoptosis gradually prevailed. Therefore, we established a model in which stretch-induced cell proliferation and apoptosis can be studied simultaneously.

Sensory Neuropeptides and their Receptors Participate in Mechano-Regulation of Murine Macrophages

“…In general, mechano-response of macrophages was associated with increased proliferation [38,39] but especially in C2C12 myoblasts and vascular smooth muscle cells, studies showed highly variable effects of cyclic stretch on proliferation and apoptosis. [40,41]. Furthermore, the stretch was reported to upregulate the gene expression of adhesion molecules in periodontal ligament cells [42], which was not the case in our study.…”

Glucocorticoid counteracts cellular mechanoresponses by LINC01569-dependent glucocorticoid receptor–mediated mRNA decay

“…The importance of mechanical stimuli to control cell behaviors (e.g., migration, differentiation, and proliferation) in mechanical disorder diseases has only been acknowledged recently (43,44). Unfortunately, the underlying mechanisms involved in mechanotransduction and how to target mechanical signaling cascades are largely unknown.…”

Scaffold‐free tissue‐engineered arterial grafts derived from human skeletal myoblasts

“…Mechanical stress has been reported to play crucial roles in muscle physiology and pathology 40 . A certain range of stretch stimulation increased the proliferation of mouse skeletal myoblasts, 41 whereas excessive stretch led to apoptosis 42 . Mechanical stretch was also reported to increase the protein expression of type 1 collagen in rat cardiac myoblasts 43 .…”